Molecular pattern recognition of oral epithelial cells against pathogenic organisms

由于宿主细胞响应白色念珠菌感染而产生的促炎细胞因子可能会影响免疫效应细胞的激活，因此我们在人牙龈上皮细胞（HGECs）中研究了这些机制。特别地，检查了白细胞介素（IL）-1α和IL-8的产生之间的关系，以及真菌细胞壁组分在IL-8产生中的作用。在体外培养的HGECs和C.白念珠菌共培养模型体系中，酵母菌对IL-1α和IL-8的分泌有明显的诱导作用。实时荧光定量PCR检测IL-1α和IL-8 mRNA表达水平也同时升高。而IL-1β、IL-6和TNF-α的分泌则无明显增加。重组人IL-1α可剂量依赖性地促进HGEC中IL-8 mRNA的表达，而抗IL-1α单克隆抗体预培养HGEC可显著抑制IL-8 mRNA的表达（P <0.01）。白念珠菌诱导IL-8 mRNA表达。当C.白念珠菌、α-甘露聚糖和β-葡聚糖均能促进HGEC产生IL-8（P <0.01）。这些结果表明，HGEC诱导IL-8的产生响应于C。白念珠菌感染通过IL-1α释放的自分泌机制，真菌细胞壁成分如α-甘露聚糖可能与这种细胞反应有关。

As the production of proinflammatory cytokines by host cells in response to Candida albicans infestation is likely to impact on the activation of immune effector cells, we examined these mechanisms in human gingival epithelial cells (HGECs). In particular, the relationship between the production of Interleukin (IL)-1α and IL-8, and the role of fungal cell-wall components in the production of IL-8 were examined. In an in vitro HGECs and C. albicans co-culture model system, a marked induction of IL-1α and IL-8 secretion by the yeast was observed. Concurrent increased expression of IL-1α and IL-8 mRNA was also noted by real-time PCR. In contrast, the secretion of IL-1β, IL-6 and TNF-α did not increase significantly. The addition of recombinant human IL-1α itself to HGEC culture prompted expression of IL-8 mRNA in a dose-dependent manner, whereas pre-culture of HGECs with anti-IL-1α monoclonal antibody significantly inhibited (P <0.01) the C. albicans-induced expression of IL-8 mRNA. When heat-killed C. albicans, α-mannan or β-glucan were introduced into HGEC culture, all except β-glucan increased IL-8 production (P <0.01). These results suggest that HGEC induces IL-8 production in response to C. albicans infestation through an autocrine mechanism of IL-1α release, and fungal cell-wall components such as α-mannan are likely to be associated with this cellular response.